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Biomedical subjects

A Grisk

Publications and source records attributed to A Grisk.

At least 19 recordsLinked to original sources
PubMed1989

[Biotransformation of B 24/76 in the rat, minipig, dog and man].

After oral administration of B 24/76 (1) on experimental animals (rat, minipig, dog) and human beings 11 metabolites could be isolated from urine, faeces and bile. The structure of 7 compounds was elucidated by means of TLC and MS. The investigated species are showing an analogues metabolic pattern with differences in the intensity and main metabolites. In phase II-reaction we could observe qualitative differences.

Adrenergic beta-Antagonists↗
PubMed1988

Subacute effects of propranolol and B 24/76 on isoproterenol-induced rat heart hypertrophy in correlation with blood pressure.

We compared the potential beta-receptor blocker, B 24/76 i.e. 1-(2,4-dichlorophenoxy)-3[2-3,4-dimethoxyphenyl)ethanolamino]-prop an-2-ol, which is characterized by beta 1-adrenoceptor blocking and beta 2-adrenoceptor stimulating properties with propranolol. The studies were performed using an experimental model of isoproterenol-induced heart hypertrophy in rats. A correlation of the blood pressure was neither found in the development nor in the attempt to suppress the development of heart hypertrophy with the two beta-receptor blockers. Both beta-blockers influenced the development of hypertrophy to a different, but not reproducible extent. It was possible to suppress the increased ornithine decarboxylase activity with both beta-blockers in hypertrophied hearts, but there was no effect on the heart mass. Neither propranolol nor B 24/76 could stop the changes in the characteristic myosin isoenzyme pattern of the hypertrophied rat heart. Thus, the investigations did not provide any evidence that the beta-receptor blockers propranolol and B 24/76 have the potency to prevent isoproterenol from producing heart hypertrophy.

Animals↗
PubMed1987

[The demonstration of proteolytic activity of bovine coronary arteries and the effect of drugs and other substances on it].

Intracellular neutral proteinases activity of bovine coronary arteries was demonstrated, isolated and partially characterized. The enriched crude enzyme preparation can be inhibited by diisopropylphosphofluoridate (DFP) and phenylmethylsulfonylfluoride (PMSF). The inhibitor concentration (pI50 values) by DFP and PMSF in the enzyme preparation and for trypsin are very similar. Several drugs (isoproterenol, propranolol, theophylline) tested on the enriched crude neutral proteinases preparation showed stimulatory or inhibitory activities. The results are discussed with regard to a possible action mechanism such proteinases on the cyclic AMP/cyclic GMP system.

Animals↗
PubMed1986

Myosin isoenzymes in normal and hypertrophied human hearts.

Distinct myosin isoforms were identified from the ventricles and atria of foetal, normal and hypertrophied human hearts. Ventricle and atrium myosins cannot be differentiated by their sedimentation behaviour in the analytical ultracentrifuge, they vary, however, with regard to the Ca2+-dependent ATPase and also the activation parameters in measurements of the enzyme activity in dependence on temperature. In agreement with other authors we observed a foetal light chain in the ventricular tissue of the latter half of gestation, when myosin was characterized by SDS-polyacrylamide gel electrophoresis and isoelectric focusing. Using pyrophosphate gel electrophoresis an additional foetal isomyosin was observed besides the typical ventricular myosin HV-3, which migrates faster. Two distinct myosin isoforms designated as HA-3 and HA-1 occur in the atrium of the normal human heart. It was found that besides their own isoenzymes normal atria also contain ventricular isomyosin, whose relative proportion is markedly increased in the hypertrophic atrium. In contrast, we usually observed only one isoenzyme in the normal ventricle. Moreover, in case of myocardial infarction a dramatic transformation of myosin heavy chain composition with a shift to an atrial myosin type took place in the ventricle.

Adult↗
PubMed1985

[Renal excretion of dimethylphosphate and its thio-derivatives following application of dimethoate, bromophos, naled or trichlorfon to rats].

Dimethoate, bromophos, naled or trichlorophon were applied i.p. or p.o. to rats in 3 doses each differing by the factor 10. In the urine of 24 h gas chromatographic determination of dimethylphosphate (DM), O.O-dimethylthiophosphate (TP), and/or O.O-dimethyldithiophosphate (DT) were carried out. After i.p. application of dimethoate the excretion rate of DT calculated from the dates found with the lowest dosage differed significantly from those found with the two other doses (t-test; p = 0.01). The excretion rates of DM and TP, in the same way, or those of DM, TP, and DT after oral intake of dimethoate did not show any significant differences. The excretion rates of TP after bromophos and of DM after naled or trichlorophon did not differ significantly after the same way of application. The findings make evident that under the given test conditions the excretion rate of DM, TP, or DT is practically independent on the dose.

Animals↗
PubMed1983

[Characterization of cyclic AMP-dependent protein kinase from smooth muscle of cattle and its modification by drugs].

Cyclic AMP-dependent protein kinase activity (ATP: protein phosphohydrolase, EC 2.7.1.37) from the postmicrosomal supernatant (100 000 X g supernatant) of bovine coronary and carotid arteries was isolated by ammonium sulfate precipitation followed by ion-exchange chromatography on DEAE-cellulose and partially characterized. Kinase activity was assayed in a standard system with [gamma-32P]-ATP and protamine at pH 7.5, 310 K, in the presence and absence of cyclic AMP. The apparent Km-values for ATP, Mg2+ and cAMP are 6.1 X 10(-5) M, 6.4 X 10(-4) M, 3.4 X 10(-8) M, respectively (coronary arteries) or 5.0 X 10(-5) M, 1.02 X 10(-3) M, 1.7 X 10(-8) M, respectively (carotids). Optimal concentrations of cAMP produced a 2-3-fold increase in the cyclic AMP-dependent protein kinase activity. After purification on DEAE-cellulose three peaks of cyclic AMP-dependent protein kinase activity were found. Especially the second peak fraction showed high protein kinase activity, strong [3H]cAMP-binding and high sensitivity to cAMP. Several drugs tested on the crude enzyme preparation showed stimulating or inhibitory activities in the concentration range of 1-10 microM.

Adenosine Triphosphate↗
PubMed1980

Acute and cutaneous toxicity of beta-chlorovinyl ketones and aldehydes in rodents.

The acute toxicity (LD50, intraperitoneal in the mouse) of beta-chlorovinyl ketones and aldehydes used as intermediates for organic syntheses was determined and their action on the skin of rodents investigated. Ketones of the type Cl-CH-CH-COR prove to be relatively toxic and display a markedly necrotic action after percutaneous absorption. In comparison with this the isomeric aldehydes Cl-CR-CH-CHO have a lower acute and less markedly cutaneous toxicity. As therapeutic counter action after skin contamination by beta-chlorovinyl carbonyl compounds the immediate treatment with an aqueous ethanolic solution of hexamethylenetetramine is recommendable.

Administration, Topical↗
PubMed1979

[Acute and subchronic experiments on the effects of microcrystalline cellulose on various pharmacological and biochemical parameters in mongrel rabbits].

The subchronic intravenous application of microcrystalline cellulose (MCC), in a dose of 5 mg/kg twice weekly for 10 weeks, resulted in servere crystal embolism in the lungs of the animals. The clinical parameters were either unchanged (erythrocyte and leucocyte counts, differential blood picture, osmotic resistance of the erythrocytes, total serum bilirubin, serum protein and serum protein fractions) or slightly pathological (hemoglobin content, hematocrit, GOT and GPT). The results from tests of the liver function (by means of bromosulphthaleine clearance) and of the renal function as well as the ophthalmologic examination were not indicative of damaged parenchyma or disturbed microcirculation. Intra-arterial infusions of MCC affected the peripheral muscular blood supply, blood pressure and heart rate.

Animals↗
PubMed1978

[Correlations between chemical structure and cardiac effectivity of a group of beta-receptor blockaders].

13 compounds from the families of halogenated phenylethanolamines and phenoxypropanol-amines were tested for their antagonistic effect against an isoproterenol-induced increase in heart rate and lowering of blood pressure, and the AD50 values were determined. All the substances had beta-adrenolytical effects. 2.4-Difluoroisoproterenol and 1-(2.4-dichlorophenoxy)-3-t-butylaminopropanol-(2) showed a higher affinity to the beta1-receptors of the heart than to the beta2-receptors of the vessels. Correlations existing between chemical structure and action on the adrenergic beta-receptors are described.

Adrenergic beta-Antagonists↗
PubMed1976

[Structure-activity relationships of halogenated phenylethanolamine and phenoxypropanolamine].

12 compounds from the series of halogenated phenylethanolamines and phenoxypropanolamines were tested at the isolated rabbit jejunum, and the pD2-and pA2-values were determined. All the substances act beta-adrenolytically. Except for 3,4-dichloronoradrenaline, which stimulates the alpha-receptors, all the compounds still have pronounced beta-mimetic effects. The 2,5-dihalogenated phenylethanolamines and phenoxypropanolamines block the beta-receptors at lower concentrations than 2,4-dihalogen derivatives. The weakest beta-adrenolytic effects at the intestine were found with compounds halogenated at the 3,4-position.

Adrenergic beta-Antagonists↗
PubMed1976

Some properties of adenosine deaminase from vascular smooth muscle and its inhibition by various vasodilators.

Because of some uncertainties still existing about the role of adenosine deaminase in the drug-influenced adenosine breakdown, the authors isolated this enzyme from vascular smooth muscle and studied the inhibition of its activity by some vasodilating drugs. The adenosine deaminase was purified 360-fold from bovine carotid artery by means of (NH4)2SO4-precipitation, heat treatment, and gel filtration. This enzyme behaves in a similar way as preparations of the same enzyme from other tissues in respect to pH-dependence and Michaelis constant. The vascular enzyme is inhibited by dipyridamole and trapymine in a competitive manner, hexobendine and lidoflazine are without any effect. The results lead to the conclusion that the inhibition of vascular adenosine deaminase does not constitute the sole cause of the adenosine-potentiating effect of the vasodilating drugs studied.

Adenosine Deaminase↗
PubMed1976

[The effect of diisopropylfluorphosphate on the adenylate cyclase activity and the 3',5'-AMP content of myocardium and brain].

Adenylate cyclase [ATP-pyrophosphatelyase (cyclizing) EC 4.6.1.1.] from ventricular muscles and the cerebrum of rats can be inhibited by diisopropylphosphofluoridate (DFP) and paraxone in concentrations from 10(-7) - 10(-9)M, and by dimethoate in concentrations from 10(-5) - 10(-7)M. The cAMP content in the heart diminished after i.p. 1.44 mg/kg DFP by 59.9%, and in the cerebrum by 68.2%. The depletion of cAMP caused by double LD50 DFP in the rat heart can be influenced neither by atropine alone, nor in combination with TMB-4. The results are discussed with regard to a possible action mechanism.

Adenylyl Cyclases↗